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Biomedical subjects

P Eriksson

Publications and source records attributed to P Eriksson.

222 records · Page 13Linked to original sources

Glucocorticoid-regulated adipose tissue secretion of PAI-1, but not IL-6, TNFalpha or leptin in vivo.

OBJECTIVE: Glucocorticoids are well-known regulators of adipose tissue metabolism and endocrine function. The aim of this study was to examine glucocorticoid effect on plasminogen activator inhibitor 1 (PAI-1), tumour necrosis factor alpha (TNFalpha), leptin and interleukin-6 (IL-6) adipose tissue secretion. MATERIAL AND METHODS: Twelve healthy postmenopausal women with mean BMI of 28.9 kg/m(2) (+/- 0.8 SEM) received 25 mg prednisolone daily for 7 days. Before and after glucocorticoid treatment adipose tissue secretion of PAI-1, leptin, IL-6 and TNFalpha were measured, and adipocyte PAI-1 mRNA as well as anthropometrical and bio-chemical data were obtained. RESULTS: Anthropometric measurements remained unaffected. Analyses of venous blood-samples showed a borderline increase of insulin levels (p = 0.062). PAI-1 secretion from adipose tissue increased (1.9 +/- 0.2 vs. 3.5 +/- 0.5 ng/g triglycerides, p = 0.012), but PAI-1 mRNA levels did not (0.19 +/- 0.02 vs. 0.21 +/- 0.04 arbitrary units after normalised to beta-actin, p = 0.51). There were no apparent differences in IL-6, TNFalpha or leptin secretion after glucocorticoid exposure. CONCLUSION: This study shows an increased secretion of PAI-1, but not IL-6, TNFalpha or leptin, from abdominal adipose tissue after in vivo glucocorticoid treatment, which may be a finding of pathophysiological importance given the well-known effect of glucocorticoid excess on metabolic aberrations and cardiovascular morbidity.

Adipose Tissue↗

Diabetes-induced changes in the Gi-modulated muscarinic receptor-adenylyl cyclase system in rat myocardium.

The inhibitory guanine nucleotide binding regulatory protein (Gi)-mediated muscarinic receptor-adenylyl cyclase system was studied in myocardium from adult male Wistar rats with 10 weeks of diabetes induced by a single intravenous injection of streptozotocin (60 mg/kg). Neither the messenger ribonucleic acid level nor the amount of Gi was changed in the streptozotocin diabetic group as compared to the control group. The activity of the adenylyl cyclase stimulated by guanyliminodiphosphate was decreased by 48% in the streptozotocin diabetic group whereas stimulated activities of adenylyl cyclase by sodium fluoride and forskolin remained unchanged. The inhibition of forskolin-stimulated adenylyl cyclase activity by carbachol was more potent in membranes from the streptozotocin diabetic group than that in membranes from the control group. The competition binding curve between (3H)- quinuclidinyl benzilate and carbachol obtained from the streptozotocin diabetic group was shifted to the left as compared to the control group. These results suggest that the myocardium of streptozotocin-induced diabetic rats exhibited an increase in Gi function as demonstrated by the increased inhibition of guanyliminodiphosphate-mediated adenylyl cyclase and the superhigh affinity for carbachol of the muscarinic receptors. As there were signs, similar to those seen in clinical heart failure, in the streptozotocin diabetic group, these results demonstrate that functional alteration of Gi might underlie, at least in part, the cardiac dysfunction that is associated with diabetes.

Adenylyl Cyclases↗

Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings.

An environmental mischance commonly occuring in nature is the combination of neonatal exposure and later adult exposure to various toxic substances. During neonatal life, offspring can be affected by toxic agents either by transfer via mother's milk or by direct exposure. In many mammalian species the perinatal period is characterized by a rapid development of the brain--'the brain growth spurt' (BGS). We have observed that exposure to pesticides, such as DDT and bioallethrin, during the BGS in mice can potentiate susceptibility to bioallethrin or paraoxon in adult life. This combined neonatal and adult exposure caused spontaneous behavioural aberrations and changes in muscarinic cholinergic receptors and led to impairment of the faculties of learning and memory. Our studies indicate that neonatal exposure to pesticides--even in low doses--can potentiate and/or modify the reaction to adult exposure to xenobiotics, and thereby accelerate dysfunctional processes.

Animals↗

Histopathology of renal biopsies with correlation to clinical findings in primary Sjögren's syndrome.

OBJECTIVE: To characterise the renal histopathological lesions in patients with primary Sjögren's syndrome and to correlate the findings with the clinical manifestations. METHODS: Kidney and labial salivary gland biopsies from ten patients with primary Sjögren's syndrome were studied. The protocol included semiquantitative assessments of the inflammatory focus scores and the levels of atrophy, interstitial fibrosis, glomerular sclerosis and vessel wall thickening. RESULTS: No statistically significant correlation was found between the kidney and labial inflammatory scores; this was probably the result of observation of the lesions at different stages. The level of chronic tubulointerstitial nephritis was correlated to the glomerular filtration rate and to the extent of glomerular sclerosis but not to vessel wall thickening. These findings indicate a primary injury of the tubules in primary Sjögren's syndrome that secondarily compromises the glomeruli. CONCLUSION: A semiquantitative approach to the assessment of histopathological features, as used in this study, appears to be valuable for characterising the lesions in kidney biopsies.

Adult↗

Transcutaneous electrical nerve stimulation in unstable angina pectoris.

BACKGROUND: Silent ischemia is a strong predictor of unfavorable outcome in unstable angina pectoris. Dynamic continuous vector cardiography provides online detection of ischemic episodes. Transcutaneous electrical nerve stimulation (TENS) has been reported to have antianginal effects in patients with severe coronary artery disease and this is associated with a reduction in myocardial ischemia. The aim of the present study was to investigate the applicability of TENS in patients with unstable angina in the coronary care unit and the effects on vector cardiographic and biochemical markers of ischemia. METHODS: Thirty patients (14 in the TENS group and 16 in a placebo group) were included in a single-blind, placebo-controlled study after being admitted to the coronary care unit. Continuous vector cardiography, leakage of cardiac enzymes and consumption of analgesics were recorded for 24 h. RESULTS: TENS was well tolerated and did not interfere with standard treatment, although vectorcardiographic recording during actual stimulation was disturbed. There was a reduction in the number of silent ischemic ST change vector magnitude episodes (P = 0.02) and their duration (P = 0.01) in the TENS-treated group, and a nonsignificant reduction in the total number of ST change vector magnitude (painful plus silent) episodes (P = 0.09) and their duration (P = 0.05) and in leakage of cardiac enzymes (P = 0.12). There were no detectable differences in terms of episodes of pain leading to stimulation or consumption of analgesics. CONCLUSIONS: TENS seems to be a safe additional treatment in unstable angina pectoris and may reduce the number of ischemic events, by mechanisms apparently unrelated to the reduction of pain.

Aged↗